There are numerous and varied causes of heart failure.[1][2]

Common causes of chronic heart failure include:

  • Coronary artery disease

  • Hypertension

  • Valvular disease

  • Myocarditis.

Other causes include:

  • Infiltrative diseases: amyloidosis, hemochromatosis, sarcoid

  • Congenital heart diseases

  • Pericardial disease

  • Toxin-induced: heroin, alcohol, cocaine, amphetamines, lead, arsenic, cobalt, phosphorus

  • Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease), parasite (e.g., Trypanosoma cruzi [Chagas disease])

  • Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with hypocalcemia, pheochromocytoma, acromegaly, growth hormone deficiency

  • Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa, hypersensitivity vasculitis, Takayasu syndrome, polymyositis, reactive arthritis

  • Chemotherapy-induced: for example, adriamycin, trastuzumab

  • Nutritional deficiencies: thiamine, protein, selenium, L-carnitine

  • Pregnancy: peripartum cardiomyopathy

  • Familial cardiomyopathy

  • Tachycardia-induced cardiomyopathy

  • Stress cardiomyopathy.

Although Chagas disease is an uncommon cause of congestive heart failure in Europe and North America, it is an important cause of heart failure in Central and South America.[2][9]

Some of these conditions tend to increase metabolic demand, which may not be matched by a sufficient increase in cardiac output by the failing heart. Tachyarrhythmias also decrease the diastolic ventricular filling time and increase myocardial oxygen demand. Uncontrolled hypertension depresses systolic function by increasing the afterload against which the failing ventricle must pump blood, and may be the first clinical manifestation. It should be emphasized that many of these causes may be completely reversible given appropriate and timely treatment/intervention (e.g., revascularization for stunned or hibernating myocardium; standard therapy for peripartum or hypertensive cardiomyopathy; valvuloplasty or valve replacement for valvular heart disease; standard treatment and adjunctive rate control therapy for tachycardia-induced cardiomyopathy and cardiomyopathy related to sepsis and stress).[2][10][11] Other causes, such as scarred myocardium or infiltrative cardiomyopathy, are currently considered irreversible.


The understanding of the pathophysiology of heart failure has evolved significantly over the last decades, from the hemodynamic model to the neurohormonal paradigm.[12] Heart failure represents a complex syndrome in which an initial myocardial insult results in the over-expression of multiple peptides with different short- and long-term effects on the cardiovascular system. Neurohormonal activation is recognized to play a pivotal role in the development as well as the progression of heart failure. In the acute phase, neurohormonal activation seems to be beneficial in terms of maintaining adequate cardiac output and peripheral perfusion. Sustained neurohormonal activation, however, eventually results in increased wall stress, dilatation, and ventricular remodeling, which contribute to disease progression in the failing myocardium, which eventually leads to further neurohormonal activation. Left ventricular remodeling is the process by which mechanical, neurohormonal, and possibly genetic factors alter ventricular size, shape, and function. Remodeling occurs in several clinical conditions, including myocardial infarction, cardiomyopathy, hypertension, and valvular heart disease; its hallmarks include hypertrophy, loss of myocytes, and increased interstitial fibrosis. One potential deleterious outcome of remodeling, as the left ventricle dilates and the heart assumes a more globular shape, is the development of mitral regurgitation. Mitral regurgitation results in an increasing volume overload on the overburdened left ventricle that further contributes to remodeling and progression of disease and symptoms.


American College of Cardiology/American Heart Association stages of heart failure[2]

This staged classification underscores the fact that established risk factors and structural abnormalities are necessary for the development of heart failure, recognizes its progressive nature, and superimposes treatment strategies on the fundamentals of preventive efforts. Heart failure may progress from stage A to stage D in a given patient, but generally does not follow the path in reverse.

  • Stage A: patients at high risk of developing heart failure because of the presence of conditions that are strongly associated with the development of heart failure (for example, hypertension, diabetes, or coronary disease); however, such patients have no identified structural or functional abnormalities of the pericardium, myocardium, or cardiac valves and have never shown signs or symptoms of heart failure.

  • Stage B: patients who have developed structural heart disease that is strongly associated with the development of heart failure but who have never shown signs or symptoms of heart failure (for example, asymptomatic post-infarction left ventricular dysfunction).

  • Stage C: patients who have current or prior symptoms of heart failure associated with underlying structural heart disease.

  • Stage D: patients with advanced structural heart disease and marked symptoms of heart failure at rest despite maximal medical therapy and who require specialized interventions (for example, heart transplant or left ventricular assist devices).

Framingham criteria for the diagnosis of CHF[3]

Heart failure is essentially a clinical diagnosis. Clinical criteria for diagnosing heart failure, the Framingham criteria for the diagnosis of CHF, were established before the widespread use of echocardiographic assessment of systolic and diastolic dysfunction. The Framingham clinical criteria, listed below, have been extremely useful for identifying heart failure patients, both in clinical practice and in epidemiologic studies, for more than 40 years. However, because their specificity is greater than their sensitivity, it is recognized that they probably miss mild cases of heart failure. In order to come up with a definite diagnosis of CHF, one needs to have either 2 major criteria or the combination of 1 major and 2 minor criteria.

Major criteria:

  • Neck vein distention

  • Rales

  • Acute pulmonary edema

  • S3 gallop

  • Increased venous pressure greater than 16 cm of water

  • Circulation time greater than 25 seconds

  • Hepatojugular reflux

  • Cardiomegaly

  • Paroxysmal nocturnal dyspnea or orthopnea.

Minor criteria:

  • Ankle edema

  • Night cough

  • Dyspnea on exertion

  • Hepatomegaly

  • Pleural effusion

  • Less than one third maximum vital capacity

  • Tachycardia (heart rate >120 bpm).

Major or minor criteria:

  • Weight loss greater than 4.5 kg in 5 days in response to treatment

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